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PMA1-containing extracellular vesicles of triggers immune responses and colitis progression.
Gut Microbes
December 2025
Department of Oncology, Nanjing Drum Tower Hospital, State Key Laboratory of Pharmaceutical Biotechnology, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.
() exhibits aberrant changes in patients with colitis, and it has been reported to dominate the colonic mucosal immune response. Here, we found that PMA1 expression was significantly increased in from patients with IBD compared to that in healthy controls. A Crispr-Cas9-based fungal strain editing system was then used to knock out PMA1 expression in .
View Article and Find Full Text PDFStreptococcal Toxic Shock Syndrome (STSS) Secondary to Monoarticular Septic Arthritis Leading to Multiorgan Failure in a Patient without Underlying Comorbidities: Emphasizing Early Diagnosis and Management Strategies.
Infect Disord Drug Targets
January 2025
HCA Healthcare Las Palmas/Del Sol Internal Medicine Program.
Background: Streptococcal Toxic Shock Syndrome (STSS) is a life-threatening condition caused by bacterial toxins. The STSS triad encompasses high fever, hypotensive shock, and a "sunburn-like" rash with desquamation. STSS, like Toxic Shock Syndrome (TSS), is a rare complication of streptococcal infec-tions caused by Group A Streptococcus (GAS), Streptococcal pyogenes (S.
View Article and Find Full Text PDFAn extracellular vesicle based hypothesis for the genesis of the polycystic kidney diseases.
Extracell Vesicle
December 2024
The Jared Grantham Kidney Institute at the University of Kansas Medical Center, Department of Nephrology and Hypertension, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Autosomal dominant polycystic kidney (ADPKD) disease is the commonest genetic cause of kidney failure (affecting 1:800 individuals) and is due to heterozygous germline mutations in either of two genes, and . Homozygous germline mutations in are responsible for autosomal recessive polycystic kidney (ARPKD) disease a rare (1:20,000) but severe neonatal disease. The products of these three genes, (polycystin-1 (PC1 4302(3)aa)), (polycystin-2 (PC2 968aa)) and (fibrocystin (4074aa)) are all present on extracellular vesicles (EVs) termed, PKD-exosome-like vesicles (PKD-ELVs).
View Article and Find Full Text PDFMolecular mechanism of aberrant decidualization in adenomyosis leading to reduced endometrial receptivity.
Front Endocrinol (Lausanne)
January 2025
Department of Gynecology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Patients with adenomyosis not only experience a decrease in quality of life as a result of dysmenorrhea and severe monthly flow but they are also rendered infertile. Pregnancy rates are still low among women with adenomyosis, even with assisted reproduction. According to the current study, endometrial receptivity is primarily responsible for the lower conception rate among patients with adenomyosis.
View Article and Find Full Text PDFPotential implications of granzyme B in keloids and hypertrophic scars through extracellular matrix remodeling and latent TGF-β activation.
Front Immunol
January 2025
International Collaboration on Repair Discoveries (ICORD) Centre, Vancouver Coastal Health Research Institute (VCHRI), University of British Columbia (UBC), Vancouver, BC, Canada.
Keloid scars (KS) and hypertrophic scars (HS) are fibroproliferative wound healing defects characterized by excessive accumulation of extracellular matrix (ECM) in the dermis of affected individuals. Although transforming growth factor (TGF)-β is known to be involved in the formation of KS and HS, the molecular mechanisms responsible for its activation remain unclear. In this study we investigated Granzyme B (GzmB), a serine protease with established roles in fibrosis and scarring through the cleavage of ECM proteins, as a potential new mediator of TGF-β activation in KS and HS.
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